There are approximately 25 million people in the U.S. with implanted, inserted or transcutaneous medical devices (see, for example, Hanna, K. E., Institute of Medicine (U.S.) Innovation and invention in medical devices: workshop summary. Washington, D.C: National Academy Press; 2001. Roundtable on Research and Development of Drugs B, and Medical Devices). The expected U.S. demand for such devices is increasing at 8% each year (see, for example, The Freedonia Group, Cleveland, Ohio, USA: Freedonia; 2010, Implantable Medical Devices to 2014—Demand and Sales Forecasts, Market Share, Market Size, Market Leaders). These devices include, but are not limited to, cardiac pacemakers, defibrillators, vascular grafts, dental implants, bone screws, catheters, coronary artery stents, staples, wires, shunts and joint replacement devices.
Although many medical devices perform adequately for years, implantation, insertion or transcutaneous placement of biomaterials and medical devices elicits a dynamic host inflammatory response (see, for example, Anderson, J. M., et al., Foreign body reaction to biomaterials, Semin Immunol 2008; 20(2):86-100, N. Broggini, L. M. McManus, J. S. Hermann, R. Medina, R. K. Schenk, D. Buser, and D. L. Cochran, Peri-implant inflammation defined by the implant-abutment interface, J Dent Res 85(5):473-478, 2006) that severely limits the integration and long-term performance of many medical devices, including joint prostheses, chemical biosensors, electrical leads/electrodes, therapeutic delivery systems, and tissue-engineered constructs, affecting millions of patients each year.
One important example with severe life threatening consequences is coronary stent implants. Coronary stents are frequently used subsequent to balloon angioplasty in order to maintain adequate coronary muscle blood flow. However the use of coronary stents fundamentally alters the vascular response to injury by causing an intense and prolonged inflammatory state (see, for example, Welt, F. and Rogers, C., Arterioscler Thromb Vasc Biol, 2002; 22: 1769-1776). This inflammatory condition causes smooth cell proliferation within the coronary artery walls as a result of damage and removal of the endothelial cell layer that lines the lumen of these vessels. Up to 60% of stent implantation results in restenosis.
A medical device that is improved such that the inflammatory response associated with its implantation, insertion or transcutaneous placement is prevented or down-regulated would have a huge impact on the success of implanted, inserted or transcutaneous devices (A W Bridges, and A J Garcia, Anti-Inflammatory Polymeric Coatings for Implantable Biomaterials and Devices, Journal of Diabetes Science and Technology, 2, (6):984-994, 2008). It is an object of the invention described below to provide such an improved medical device.